Pollution exposure during pregnancy can cause chromosomal abnormalities in fetal tissues

Feb 23 2005

A new study of newborns in New York City reveals that prenatal exposure to combustion-related urban air pollutants alters the structure of chromosomes (the carriers of genes) of babies in the womb.

This is the first study to show that environmental exposure during pregnancy to such pollutants can cause a modest but significant increase in chromosomal abnormalities in fetal tissues. Such genetic alterations have been linked in other studies to increased risk of cancer in children and adults.

The study was released today by the Columbia Center for Children's Environmental Health, part of the Mailman School of Public Health at Columbia University. The results of the study will be published in Cancer Epidemiology Biomarkers and Prevention, a prominent, peer-reviewed scientific journal, and also are available online.

The research involved a sample of 60 newborns and their non-smoking mothers in low-income neighborhoods of New York City ( Harlem, Washington Heights and the South Bronx). The mothers' exposure during pregnancy to varying levels of airborne combustion-related pollutants, known as polycyclic aromatic hydrocarbons (PAHs), was measured by personal air monitoring of the mothers during pregnancy. PAHs are carcinogenic air pollutants that cross the placenta. They enter the environment when combustion occurs -- such as from car, truck or bus engines, residential heating, power generation or tobacco smoking.

"We have previously learned that air pollutants significantly reduce fetal growth, which may affect cognitive development during childhood, but this is the first evidence that they can alter chromosomes in utero," said Frederica P. Perera, director of the center and principal author of the study. "This is troubling since this type of genetic alteration has been linked in other studies to increased risk of cancer. While we can't estimate the precise increase in cancer risk, these findings underscore the need for policymakers at the federal, state and local levels to take appropriate steps to protect children from these avoidable exposures."

In this study, prenatal exposure was assessed by the use of questionnaires and personal air monitors worn by the mothers during the third trimester. Chromosomal aberrations were measured in cord blood lymphocytes by fluorescence in situ hybridization, a method that allows visualization of such abnormalities. In a subset of newborns, PAH-related DNA damage also was measured in umbilical cord blood.

Airborne PAHs were significantly associated with stable aberration frequencies in cord blood. Although the frequency of these aberrations was quite low, aberrations that are stable, and therefore persistent, are of particular concern for cancer risk. In the subset of 22 newborns with detectable levels of the biomarker, PAH-DNA adducts were not associated with chromosomal aberrations, possibly because of the limited size of the subset.

The study is part of a broader, multiyear research project, "The Mothers & Children Study in New York City," begun in 1998, which examines the health effects of exposure of pregnant women and babies to air pollutants from vehicle exhaust, the commercial burning of fuels, and tobacco smoking, as well as from residential use of pesticides and allergens.